Epigallocatechin gallate inhibits angiotensin II-induced endothelial barrier dysfunction via inhibition of the p38 MAPK/HSP27 pathway.

Acta Pharmacologica Sinica
Dan YangHui-hua Li

Abstract

To investigate the effect of epigallocatechin gallate (EGCG) on angiotensin II (Ang II)-induced stress fiber formation and hyperpermeability in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were treated with Ang II in the absence or presence of EGCG or mitogen-activated protein kinases (MAPKs) inhibitors. The resulting stress fibers were stained with rhodamine-phalloidin and examined using confocal microscopy. The permeability of the endothelium was tested with fluorescein-isothiocyanate labeled bovine serum albumin (FITC-BSA), and the phosphorylation levels of several proteins were determined using Western blot analysis. Ang II (1-100 nmol/L) treatment markedly provoked stress fiber formation and hyperpermeability in HUVECs in a time- and dose-dependent manner. These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway. Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability. Our data demonstrate that EGCG inhibits Ang II-induced...Continue Reading

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